Diet‐Induced Changes in Membrane Gangliosides in Rat Intestinal Mucosa, Plasma and Brain

Park, Eek Joong; Suh, Miyoung; Ramanujam, Kal; Steiner, Kurt; Begg, David; Clandinin, Michael T.

doi:10.1097/01.mpg.0000157199.25923.64

Cited by 78 publications

(86 citation statements)

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“…Recently, the use of the SM synthesis inhibitor myriocin in apoE 2/2 mice demonstrated that plasma SM could be decreased without significant reduction of cholesterol and TG levels (19,218). Notably, the degree of arteriosclerosis was decreased in both studies.…”

Section: Effects Of Drugsmentioning

confidence: 90%

Absorption and lipoprotein transport of sphingomyelin

Nilsson

Duan

2006

Journal of Lipid Research

227

201

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Dietary sphingomyelin (SM) is hydrolyzed by intestinal alkaline sphingomyelinase and neutral ceramidase to sphingosine, which is absorbed and converted to palmitic acid and acylated into chylomicron triglycerides (TGs). SM digestion is slow and is affected by luminal factors such as bile salt, cholesterol, and other lipids. In the gut, SM and its metabolites may influence TG hydrolysis, cholesterol absorption, lipoprotein formation, and mucosal growth. SM accounts for z20% of the phospholipids in human plasma lipoproteins, of which two-thirds are in LDL and VLDL. It is secreted in chylomicrons and VLDL and transferred into HDL via the ABCA1 transporter. Plasma SM increases after periods of large lipid loads, during suckling, and in type II hypercholesterolemia, cholesterol-fed animals, and apolipoprotein E-deficient mice. SM is thus an important amphiphilic component when plasma lipoprotein pools expand in response to large lipid loads or metabolic abnormalities. It inhibits lipoprotein lipase and LCAT as well as the interaction of lipoproteins with receptors and counteracts LDL oxidation. The turnover of plasma SM is greater than can be accounted for by the turnover of LDL and HDL particles. Some SM must be degraded via receptor-mediated catabolism of chylomicron and VLDL remnants and by scavenger receptor class B type I receptor-mediated transfer into cells. Sphingomyelin (SM) in mammalian cells is colocalized with cholesterol mainly in the plasma membrane and in lysosomal and Golgi membranes. It interacts strongly with cholesterol, and the regulation of SM and cholesterol metabolism are in part coordinated (1, 2). In plasma lipoproteins, SM is the second most abundant polar lipid after phosphatidylcholine (PC). The size of the plasma lipoprotein SM pool in humans is 1-1.5 g, of which approximately two-thirds are in apolipoprotein B (apoB)-containing triglyceride (TG)-rich lipoproteins and LDL. The SM content in most extraneural tissues is 1-2 g/kg. Factors regulating plasma SM concentration have received little attention. It was early shown that the level of SM is increased in hypercholesterolemia and that SM-rich lipoproteins accumulate in arteriosclerotic lesions (3-5). Plasma SM is thus a risk factor for ischemic heart disease (6), and the apoE-deficient (apoE 2/2 ) mouse, which accumulates SM-rich remnant particles in blood (7), has emerged as an important model for studying the role of SM in atherogenesis. The effects of lipoprotein SM in the arterial wall during atherogenesis may be related both to the modification of lipoproteins and to the generation of sphingolipid messengers (i.e., ceramide, ceramide-1-phosphate, sphingosine, and sphingosine-1-phosphate) initiated by SM hydrolysis (8-10). The role of SM metabolites in cell signaling has been the subject of several recent reviews (11)(12)(13)(14)(15)(16). Sphingolipid signals are triggered by numerous stimuli and mediate effects on cell growth and apoptosis and on the activities of inflammatory cells that may be pathogenic as well as protect...

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Section: Effects Of Drugsmentioning

confidence: 90%

Absorption and lipoprotein transport of sphingomyelin

Nilsson

Duan

2006

Journal of Lipid Research

227

201

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“…Dietary gangliosides are absorbed by small intestines and transported to different receptor membranes in the body. 8 After absorbed by small intestines, dietary gangliosides may be reformed in the enterocyte, which will induce a change in the spectrum patterns of gangliosides in membranes. These gangliosides then come into blood circulation and finally cross the blood-brain barrier (BBB) (Figure 3).…”

Section: Discussionmentioning

confidence: 99%

Diet-Induced Changes in Spectrum Patterns of Serum Gangliosides in 6-Month-Old Infants

Gurnida¹,

Idjradinata²,

Muchtadi³

et al. 2012

mkb

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“…Earlier studies show that a decrease in cholesterol content increases EPL uptake in human leukemia cell lines [27]. Since experiments in our laboratory have shown a cholesterol reduction in the intestine of animals fed the SPL diet [6], it is logical to assume that dietary SPL may increase EPL uptake by decreasing intestinal cholesterol content. A recent study demonstrates that intestinal (I)-fatty acid binding protein (FABP) and liver (L)-FABP increase EPL content in CPG and EPG [38].…”

Section: Discussionmentioning

confidence: 99%

“…Our previous work demonstrates that dietary GG increases the total content of GGs and decreases cholesterol content in developing rat intestine [6]. Thus it was logical to hypothesize that dietary GG will increase the content of polyunsaturated fatty acids (PUFA) in EPL in the intestine by increasing derivatives of SPL and by decreasing cholesterol content.…”

Section: Introductionmentioning

confidence: 99%

“…Change occurs in the composition and molecular structure of GGs during intestinal development [4]. Monosialoganglioside GM3 (GM3) is the major GG in rat intestine [5] and is localized at the brush border membrane while disialoganglioside GD3 (GD3) is present at the basolateral membrane [6]. These findings imply that intestinal function may be influenced by the presence and composition of constituent sphingolipids (SPL).…”

Section: Introductionmentioning

confidence: 99%

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